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Nerve conduction defects are retarded by tight metabolic control in type I diabetes
Author(s) -
Hyllienmark Lars,
Golster Helena,
Samuelsson Ulf,
Ludvigsson Johnny
Publication year - 2001
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/1097-4598(200102)24:2<240::aid-mus90>3.0.co;2-2
Subject(s) - sural nerve , medicine , nerve conduction velocity , abnormality , diabetes mellitus , sensory nerve , metabolic control analysis , motor nerve , nerve conduction , type 2 diabetes mellitus , cardiology , surgery , sensory system , endocrinology , anatomy , neuroscience , psychology , psychiatry
This follow‐up study examines whether the development of nerve dysfunction is retarded by tight metabolic control in patients with type I diabetes mellitus. Seventy‐one patients and 115 age‐matched healthy control subjects underwent studies of nerve conduction in peroneal and sural nerves. The presence of diabetes was associated with a reduction in peroneal motor nerve conduction velocity (MCV) by 5.9 m/s, sural sensory nerve conduction velocity (SCV) by 3.4 m/s, and sural sensory nerve action potential (SNAP) amplitude by 22%. Dysfunction in peroneal MCV, sural SCV, and sural SNAP were related to long‐term poor metabolic control. Eleven of 12 patients with HbA1c <6.5% had normal nerve conduction or abnormality in only one nerve as compared to 2 of 15 patients with HbA1c >8.0%. It is concluded that tight long‐term metabolic control (HbA1c <6.5%) can retard nerve dysfunction in patients with type I diabetes mellitus and a mean disease duration of 12 years. © 2001 John Wiley & Sons, Inc. Muscle Nerve 24: 240–246, 2001